Download Nontuberculous mycobacteria in the HIV infected patient

Clin Chest Med 23 (2002) 665 – 674
Nontuberculous mycobacteria in the
HIV infected patient
Denis Jones, MD*, Diane V. Havlir, MD
School of Medicine, University of California, Mail Code 8208, 150 W. Washington Street,
#100, San Diego, CA 92103, USA
Disseminated Mycobacterium avium complex
(MAC) disease was one of the first opportunistic
infections recognized as part of the syndrome of
AIDS 20 years ago [1]. Clinicians rapidly became
familiar with the classic triad of fever; drenching
sweats, and anorexia characteristic of this previously
obscure disease [1 – 3]. Interest in disseminated MAC
and nontuberculous mycobacteria (NTM) infections
increased as a result of the HIV epidemic, and
therapeutic strategies to treat and prevent these diseases evolved over the next 15 years [4 – 6]. Prevention and treatment regimens were lifelong because
cure of NTM was not achievable in AIDS patients
with profound immune suppression.
The application of highly active antiretroviral
therapy (HAART) for the treatment of HIV disease
dramatically reduced rates of all opportunistic infections including NTM [7,8]. Despite this decline, NTM
remains one of the most commonly encountered
opportunistic infections in AIDS patients [8]. Disease
resulting from NTM now occurs in the following
settings: in patients not receiving antiretroviral therapy, in patients who are intolerant or failing antiretroviral therapy, and in the early period following the
initiation of HAART prior to immune recovery.
HAART also altered the clinical approach to MAC
and led to the recognition of new clinical syndromes.
In this article, we address the changing epidemiology of NTM, new approaches to prophylaxis and
treatment, and the newly described ‘‘immune reconsititution syndrome’’ associated with NTM.
* Correspondiung author.
E-mail address: [email protected] (D. Jones).
Mycobacterium avium complex
The Mycobacterium avium complex includes both
M avium and M intracellulare, which together
account for the majority of disease-causing species
of NTM in the HIV-infected patient. M avium is the
most common cause of NTM disease in patients with
AIDS, with serotypes 1, 4, and 8 being the most
commonly isolated [10,11]. Although there is a
geographic variation in serotypes within the United
States, MAC disease occurs in all demographic
groups and its occurrence is not influenced by gender
or HIV risk factors [12,13].
Clinical perspective on the epidemiology of MAC
MAC is environmentally acquired and is not
transmitted from human to human. MAC can be
recovered from numerous environmental sources
including water, soil, food, and animals; however, it
is not clear which source or sources are principally
responsible for human infection [13,14]. The presence of MAC in the sputum or stool of patients with
AIDS prior to the development of disseminated
disease suggests that infection results from inhalation
or ingestion [10,15,16].
Profound immunocompromise is the major risk
for the development of disseminated MAC [17]. A
number of studies demonstrate that the median CD4
cell count is consistently less than 50 cells/mm3 at the
time that disseminated disease is diagnosed. In one
prospective observational study of HIV-infected
patients cultured monthly for MAC, the incidence
of infection for patients with less than 200 CD4 cells/
mm3 was 43% after 2 years. In the subgroup of
0272-5231/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 2 7 2 - 5 2 3 1 ( 0 2 ) 0 0 0 1 5 - 1
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patients with less than 10 CD4 cells/mm3, the incidence of infection was 39% at 1 year [18]. Another
risk factor for MAC is increased HIV RNA levels.
Williams et al showed that plasma HIV RNA level
greater than 100,000 copies/ml was associated with a
threefold increase in the risk of developing MAC in
patients with CD4 < 75 cells/mm3 [19].
Other risk factors for the development of disseminated MAC appearing in the literature include exposure to hard cheeses and residence in the southern
states; however, the inability to culture MAC from
cheese and the geographic differences in the approach
to diagnosis have brought both these associations into
question [20].
One of the interesting observations of NTM disease in HIV-infected patients is the low frequency of
disease in Africa despite the presence of NTM in the
environment. Evidence of environmental exposure to
MAC occurring in humans in Africa is supported by
the finding that skin test reactivity to M avium is as
common in Kenya as it is in certain areas of the United
States [10]. A number of explanations have been put
forth to explain this observation. Comorbidities may
result in death prior to progression of HIV disease to a
state of immune compromise that is associated with
NTM disease. Another theory put forth to explain the
low incidence of disease is that exposure to other
mycobacterial pathogens such as M tuberculosis or
M bovis (in bacillus Calmette-guerin [BCG]) provides
cross-protective immunity to MAC. This theory is
supported by the low reported incidence of disease in
countries such as Sweden, where childhood vaccination with BCG was common [21 – 23].
The literature is not conclusive in terms of
explaining this NTM epidemiology in Africa. As
prophylaxis for opportunistic infections in Africa is
increasingly implemented, we may also observe
increases in NTM disease.
The most important change in the epidemiology
of NTM has been the tremendous reduction in new
cases. Disseminated MAC steadily declined over the
past decade with the most rapid decline occurring
after the introduction of HAART. Data from the
Adult/Adolescent spectrum of HIV disease project
group showed a decline in the incidence of MAC of
39.9% per year from 1996 to 1998. Palella and
colleagues described a similar decline in a cohort
of 1255 patients from 1994 to 1995 [7,8]. Other
factors partially responsible for the decline in NTM
are the improved general care of HIV infected
patients and specific preventative measures for
opportunistic infections [24]. Most cases of MAC
today occur in patients who have not accessed care;
however, it is possible that we may see an increase in
the incidence in those patients failing antiretroviral
therapy [25].
Pathogenesis in HIV-infected patients
Disseminated MAC is most likely a result of
primary infection rather than reactivation. In vitro
evidence showing that MAC can bind and invade
intestinal cell lines supports the animal models
showing that colonization of the gastrointestinal or
respiratory tracts precedes disseminated disease
[15]. The precise immune defect predisposing HIV
infected patients to disseminated disease is unknown.
In vitro, cells from HIV infected patients are able to
ingest M avium and respond to interferon gamma
[26]. Reduction in host production of cytokines, such
as interferon gamma, increased production of
M avium growth promoting cytokines, such as interleukin (IL)-6, may favor dissemination of NTM in
HIV infection [27,28].
The propensity for developing disseminated
NTM disease in HIV infected patients is dependent
not only on the level of the host’s immunity but also
on the virulence of the organism. Support for this is
found in the increased isolation of certain serotypes
in disseminated disease and the fact that transfection
of a plasmid into a nonplasmid-containing strain of
M avium is associated with increased intracellular
replication [29,30]. Intracellular survival of M avium
is enhanced by inhibition of phagosome-lysozyme
fusion, and localization of the organism to less
acidic vacuoles within the cell favors long-term
survival [31].
Similar to other opportunistic infections, the
development of MAC is associated with a more rapid
progression of HIV disease and subsequent death.
Many opportunistic infections, including disseminated M avium, activate lymphocytes. Because productive HIV infection requires cellular activation,
HIV replication increases when an opportunistic
infection develops. In one study, HIV RNA plasma
levels increased after the onset of disseminated MAC
[32]. Increased HIV replication within macrophages
has also been reported in patients with disseminated
disease [33].
Clinical manifestations
AIDS patients not receiving HAART who become
infected with MAC differ from immunocompetent
hosts in that they tend to develop disseminated disease. The most commonly encountered symptoms include fever, night sweats, anorexia, and weight loss
(Table 1). Nausea, vomiting, diarrhea (47%), and
D. Jones, D.V. Havlir / Clin Chest Med 23 (2002) 665–674
Table 1
Frequency of symptoms, physical findings, and laboratory
abnormalities among patients with disseminated MACa
Findings
Fever
Night sweats
Diarrhea
Abdominal pain
Nausea/vomiting
Weight loss
Lymphadenopathy
Intra-abdominal
Mediastinal
lymphadenopathy
Hepatosplenomegaly
Anemia ( < 8.5 g/dL)
Elevated serum
alkaline phosphatase
No. of patients
evaluated
Percentage of
positive patients
120
85
92
54
31
37
54
87
78
47
35
26
38
37
49
10
38
39
38
24
85
53
a
From Benson CA, Ellner JJ. Mycobacterium avium
complex infection and AIDS: advances in theory and practice.
Clin Infect Dis 1993;17:7 – 20.
abdominal pain (35%) are other frequently reported
symptoms. These symptoms, although classic for MAC
are nonspecific, and investigations for other AIDS
complications such as tuberculosis, fungal infections,
and malignancies are routinely performed [11].
Because of the widespread involvement of the
reticuloendothelial system, physical exam often
reveals hepatomegaly, splenomegaly and lymphadenopathy. Anemia and an elevated alkaline phosphatase
are among the more commonly reported laboratory
abnormalities [34].
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Localized forms of infection are reported in
patients with AIDS and include osteomyelitis, pancreatitis, and meningoencephalitis, as well as intraabdominal and soft-tissue abscesses [11].
Pulmonary disease occurs in fewer than 5% of
cases of disseminated disease and may occur without
evidence of dissemination. In the immunosuppressed
host, pulmonary infection has a myriad of radiographic presentations including nodules, infiltrates
(diffuse or localized), cavities, and lymphadenopathy
[35,36]. A recent series from northern Australia
suggested that the incidence of pulmonary MAC
might be higher than this, with 4 out of 15 of their
HIV-infected patients developing pulmonary manifestations [37].
Recently, a new clinical entity caused by M avium
has been described in patients with AIDS who initiate
potent antiretroviral therapy. This entity probably
represents a recovery in pathogen-specific immune
responses to infections that are already present but
not clinically detectable [9]. A number of different
names have been coined for this syndrome: immune
reconstitution syndrome, immune recovery disease,
and the paradoxical response. This syndrome has
been described in a number of infections including
M tuberculosis, cytomegalovirus, hepatitis B and C,
cryptococcosis, and MAC [9,38,39].
When this syndrome occurs as a result of MAC,
the presenting features are usually fever, lymphadenitis (mesenteric and/or cervical), and leukocytosis.
The disease present, however, with symptoms related
to any site where the infection has remained quiescent
in the absence of an adequate immune response
(Fig. 1).
Fig. 1. MR imaging shows localized Mycobacterium avium complex lesion related to immune reconstitution.
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The symptoms are often fairly mild and in most
cases will resolve with continued antiretroviral therapy. Interestingly, blood cultures are usually negative
for MAC. Should the inflammatory symptoms
be severe, a short course of corticosteroids may
be necessary.
The onset of the immune reconstitution syndrome
usually occurs within the first few weeks following
the initiation of potent antiretroviral therapy; however, its onset may be delayed for up to 1 year [40].
Although this syndrome is usually seen when
HAART is first initiated, it can occur each time the
patient is challenged with HAART.
It has been suggested by some that there may be a
genetic predisposition to the development of the
immune reconstitution syndrome. Price et al showed
that HLA B44 was associated with the development
of atypical cytomegalovirus (CMV) retinitis following the initiation of HAART [41].
Diagnosis
Colonization with MAC has been described in
both the immunocompromized as well as the immunocompetent patient. It is therefore important that
certain diagnostic criteria are met before disease is
attributed to infection with MAC [12,42].
Isolation of the organism from a normally sterile
site is often sufficient to make the diagnosis; with
blood cultures remaining one of the easiest and most
sensitive methods of diagnosing disseminated disease. A single blood culture is reported to have a sensitivity of 90 – 95%. In rare cases where the clinical
suspicion is high and blood cultures are negative, liver
or bone marrow biopsy should be considered [10,42].
A number of different culture mediums are available, the Lowenstein-Jensen being the most commonly used solid medium. Broth media allow for
the more rapid detection of mycobacteria, usually
within half the time it takes using a solid medium.
Detection of mycobacteria in broth media, such as the
BACTEC or Septi-chek system, is dependent on the
production of CO2 which is then detected radiometrically [43].
Mycobacterial detection using various DNA
probes has been a major advance over the past
decade. A variety of probes are commercially available. These DNA probes will detect numerous mycobacteria within a few hours of adequate growth in a
culture medium [44,45].
In AIDS patients, MAC is often detected in the
respiratory tract, although this finding does not
necessarily indicate disseminated infection or the
need for treatment. A thorough search for other
pathogens should be pursued before the diagnosis
of pulmonary MAC is made. Distinguishing MAC
and other tuberculous infections on a clinical basis is
very difficult because of the nonspecificity of clinical
findings. Rapid diagnostic testing for M tuberculosis
can be very helpful when a patient has acid-fast
bacilli seen on smear.
The American Thoracic Society has provided
guidelines for the diagnosis of MAC-related pulmonary disease. These guidelines are recommended for
both HIV and non-HIV infected patients [46].
Treatment
For the clinician treating disseminated MAC,
there are a number of different combinations available for treatment; however, several principles of
therapy should be observed. First, the cornerstone
of treatment is the inclusion of either clarithromycin
or azithromycin in the regimen. As single agents,
these drugs are the most potent drugs available for the
treatment of MAC. The second principle is that
treatment regimens should contain at least one additional agent to prevent the development of resistance.
Third, patients failing treatment should be tested for
drug resistance, with therapy adjusted accordingly
[5,47]. In vitro assays of drug susceptibility provide
useful information for clarithromycin and azithromycin; cutoffs for other drugs are less clear. Finally, in
the absence of immune recovery (treatment of HIV
disease with HAART) treatment of MAC should be
life-long [48].
Clarithromycin is the macrolide most often used
to treat MAC and should be prescribed at a dose of
1000 mg per day. Although higher doses result in a
more rapid clearance of bacteremia, they also have
been reported to cause more side effects and (possibly) a higher mortality [5]. Azithromycin is a
comparable alternative to clarithromycin and should
be given at a dose of 600 mg/day. Dunne et al
recently showed that azithromycin, when given at
600mg per day, is as effective as clarithromycin
dosed at 500 mg bid [49]. Tolerability is important
for patient adherence, and physicians should not
hesitate to use these agents interchangeably to
achieve maximal effect.
Ethambutol has been shown to reduce the relapse
of bacteremia when given to patients on a clarithromycin-containing regimen; hence, its choice as the
second agent in the treatment of disseminated MAC
[50,51]. Whether a third agent should be added for
the treatment of disseminated MAC is still open to
debate. Gordin et al recently showed in a study of
178 patients that there was no impact on bacterio-
D. Jones, D.V. Havlir / Clin Chest Med 23 (2002) 665–674
logic response or survival when rifabutin was added
to clarithromycin and ethambutol [52]. There was,
however, a trend to a lower incidence of resistance in
the rifabutin group.
Agents less studied include the quinolones, cycloserine, amikacin, and ethionamide. Clofazamine is no
longer recommended for the treatment of disseminated MAC. This is based on a study showing that
when clofazimine was added to clarithromycin and
ethambutol, there was no increase in efficacy and a
higher mortality [53].
Recurrence of bacteremia in a patient on an effective multidrug regimen should prompt clarithromyicn
and azithromycin susceptibility testing, and in those
patients showing resistance, two new agents should be
added [5]. Macrolide therapy should be continued,
using the principle that most patients will have a
mixed infection with some sensitive strains remaining
[54]. In patients failing MAC therapy with resistant
organisms, optimizing HIV therapy may offer the best
chance of controlling or curing the infection.
With the many benefits of antiretroviral therapy
comes the risk of drug interactions. Rifabutin, a drug
often used to treat MAC interacts with many of the
drugs used to treat HIV infection. The clinician
should be aware of the potential interactions between
the antibiotics and antiretroviral agents, as outlined
in Table 2 below.
The duration of MAC therapy in patients who are
responding to HAART is not known. In one recent
observational study, Aberg described 4 patients who
had their antimycobacterial therapy discontinued.
All four patients had responded to HAART with
absolute CD4 cell counts > 100 cells/mm3 and viral
loads < 1,0000 copies/mL, and all patients had
received more than 12 months of antimycobacterial
therapy. After follow-up (range of 8 – 13 months), all
patients remained asymptomatic with negative blood
cultures [55].
of MAC bacteremia by approximately 60% when
compared with placebo [56,57].
Although inferior to azithromycin or clarithromycin, rifabutin is acceptable when these drugs are
contraindicated. Rifabutin alone reduces the risk of
bacteremia by approximately 50% [58].
The combination of rifabutin with the macrolides
was studied as a possible means of improving prophylaxis; this combination resulted, however, in an
increase in adverse events, an increase in drug interactions, and no survival advantage. Combination
therapy can therefore not be recommended for MAC
prophylaxis [59].
Despite the proven effectiveness, prescription of
acceptable MAC prophylaxis remains suboptimal.
The Centers for Disease Control and prevention
through the ASD project showed that, by the end of
1998, only 54% of eligible persons were prescribed
prophylaxis [8].
Based on information obtained from two large
clinical trials, the 2001 USPHS/IDSA guidelines recommend that primary prophylaxis be discontinued
in patients who have responded to antiretroviral therapy and have sustained a CD4 T lymphocyte count
of greater than 100 cells/mm3 for at least 3 months
[48,60,61]. Although the CD4 count is the most important variable when considering stopping prophylaxis, other risk factors that should be considered are
Table 2a
Suggested Rifabutin dosage adjustment for anti-retroviral
therapy
Drugs interacting
with Rifabutin
Protease inhibitors
Saquinavir
Nelfinivir
Indinavirb
Amprenavir
Ritonivir
Prophylaxis
MAC prophylaxis should be initiated in patients at
high risk for MAC in whom disseminated disease is
not present. If rifabutin is required, active tuberculosis
should be excluded before this drug is initiated.
The United States Public Health Service/Infectious Diseases Society of America (USPHS/IDSA)
guidelines advise that all patients who are HIV
infected with CD4 counts < 50 cells/mm3 receive
preventative therapy for disseminated MAC [48].
The most commonly used regimens are azithromycin 1200 mg once weekly or clarithromycin
500 mg twice daily. Both agents reduce the incidence
669
Lopinavir ritonivir
NNRTIS
Delavirdine
Nevirapine
Efavirenz
Alteration in the dose of
Rifabutin from 300 mg daily
No change required
Decrease to 150 mg daily
Decrease to 150 mg
twice weekly
Avoid concomitant use
No change needed
Increase to 450 mg
NNRTIS, non-nucleoside reverse transcriptase inhibitor.
a
USPHS/IDSA. 2001 USPHS/IDSA guidelines for the
prevention and treatment of opportunistic infections in
persons infected with human immunodeficiency virus,
revision 13. 2001, p. 1 – 64.
b
In addition to the suggested changes to Rifabutin
dosing, the USPHS/IDSA guidelines suggest increasing
Indinavir dosing to 1000 mg q8h when these 2 agents are
used together.
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D. Jones, D.V. Havlir / Clin Chest Med 23 (2002) 665–674
the current viral load and the CD4 nadir. Patient
compliance with continued antiretroviral therapy as
well as the availability of an effective treatment
regimen should also weigh in the decision of whether
or not to stop prophylaxis.
Nontuberculous mycobacteria other than MAC
Most NTM disease in HIV-infected patients other
than MAC is caused by M kansasii [62]. Some of the
other NTM encountered in HIV-infected patients
include M chelonei, M fortuitum M gordonae, M malmoense, M marimum and M xenopi. All of these organisms are capable of causing disseminated disease
with a symptom complex resembling MAC [10].
These organisms are often contaminants or colonizers; however, when the typical symptoms are
present, isolation of one of these organisms from a
normally sterile site provides strong evidence for a
true infection.
M kansasii
M kansasii is the second most common cause of
nontuberculous pulmonary disease in the United
States and causes a clinical and radiographic picture
that closely resembles M tuberculosis [62]. Despite
this similarity, there is little evidence of human-tohuman transmission. The source of infection remains
unclear, although the presence of the organism in tap
water has been well documented [63].
M kansasii infection usually occurs in severely
immunosuppressed patients (CD4 counts >50 cells/
mm3) and typically presents with isolated pulmonary
disease ( ± 70%). Disseminated disease is less common than that seen in MAC, with only approximately
20% having only extrapulmonary manifestations.
Those with disseminated disease were typically the
most severely immunocompromised [10].
Clinical presentation
Symptoms seen in M kansasii infections are
usually those encountered in patients with tuberculosis and include fever, cough, night sweats, and
weight loss. Chest pain and hemoptysis are less
common than in tuberculosis. In addition to those
symptoms mentioned, disseminated disease often
features lymphadenopathy, hepatosplenomegaly,
osteomyelitis, and cutaneous lesions [64].
Radiographic findings
Radiographically, the disease is most often seen in
the upper lobes and manifests as multiple cavities of
varying sizes with associated volume loss. Disease is
most often unilateral, with bilateral disease reported
in approximately 40% of cases [62,63].
Although it is almost impossible to distinguish
M kansasii from M tuberculosis on the chest radiograph, some features suggestive that M kansasii is the
responsible organism include thin walled cavities,
smaller cavities, and a higher incidence of pre-existing
lung disease.
Diagnosis
The diagnosis of M kansasii requires either the
isolation of the organism from a sterile site or, in the
case of pulmonary disease, the American Thoracic
Society (ATS) criteria should be met. These are the
same criteria that were outlined earlier for the diagnosis of MAC-related pulmonary disease [46].
DNA probe technology was initially thought to
be a poor tool for the identification of M kansasii. It
was the failure of the earlier probes to identify all
groups within the M kansasii species that led to false
negatives and, hence, this opinion. Reformulated
versions of Accuprobe (Gen Probe Inc, San Diego,
CA) have overcome this problem and are now widely
used for the identification of M Kansasii [65,66].
Treatment
The ATS recommends a combination of isoniazid
(INH), rifampin, and ethambutol for a period of
18 months or until the cultures have been negative
for a minimum of 12 months [46]. Pyrazinamide
(PZA) should be avoided because of widespread
resistance of the organism; INH on the other hand
can often be used despite resistance on susceptibility
testing. The reason for this is that many isolates are
resistant at concentrations of 1ug/mL but sensitive at
concentrations of 5ug/mL which are similar to those
found in vivo [10].
Other agents with activity against M kansasii include streptomycin, clarithromycin, sulfamethoxazole,
and certain quinolones.
M gordonae
M gordonae is a ubiquitous organism and is usually considered a contaminant when recovered in culture. Although considered to be an organism with
low pathogenicity, there have been reports of both
D. Jones, D.V. Havlir / Clin Chest Med 23 (2002) 665–674
pulmonary and disseminated disease in the immunocompromised host [67].
Relating disease to M gordonae requires that the
same criteria be met as for other NTM.
The pulmonary presentation of M gordonae does
not appear to have any typical presentation; a recent
study of 19 patients all with sputum positive for
M gordonae failed to show any typical radiographic
features [68]. Although the clinician is often unable to
distinguish the type of NTM from the chest radiograph, the finding most commonly noted in AIDS
patients with NTM (excluding M kansasii) is an
interstitial pattern that may be localized or diffuse.
Cavitary disease has been reported to be very rare in
this immunosuppressed population. The treatment
usually requires a multidrug regimen with rifampin
and ethambutol making up the core of the regimen.
671
from Bellevue Hospital, they reported that, following
the introduction of the MGIT (mycobacterial growth
indication tube) system, the number of isolated cases
increased from 12 cases in the 4 years prior to the
introduction of the system to 381 cases in the 4 years
following the introduction [71].
The clinical features of M xenopi infection in
the HIV-infected patient include both disseminated
disease and pulmonary manifestations. Pulmonary
disease typically occurs in those with pre-existing
pulmonary disease.
The treatment usually includes a combination of
INH, rifampin, ethambutol, and streptomycin. In a
study of non-HIV infected patients, the addition of
INH to a regimen of rifampin and ethambutol resulted
in lower relapse rates and less treatment failure [72].
Other mycobacteria
M genavense
M genavense is a newly recognized pathogen in
HIV-infected patients. It was first described in a
patient with AIDS in 1990 [69]. Its incidence is
probably similar to other NTM with Monill et al
reporting 8 cases of M genavense over a 5-year
period, with these cases comprising 9% of the
NTM infections in their institution [70]. Some investigators have suggested that the true prevalence may
be underestimated because of difficulties experienced
when culturing the organism.
Patients infected with M genavense are usually
severely immunocompromised (average CD4 count
of 50 cells/mm3) and present with nonspecific symptoms of fever, wasting, abdominal pain, and diarrhea.
Physical findings include hepatosplenomegaly, anemia, and abdominal lymphadenopathy. Pulmonary
involvement is rare, if it exists at all.
The findings on abdominal CT scan are also
nonspecific with lymphadenopathy (retroperitoneal,
mesenteric, and peri-pancreatic), splenomegaly and
diffuse proximal small bowel thickening being the
most well-described features [70].
Treatment has not been well studied, although
success with macrolide-based regimens similar to
those used for MAC has been reported [10].
M xenopi
M xenopi is a commonly found organism and is
often considered a contaminant. Reports of an
increasing incidence are probably the result of more
sensitive tests becoming available. In a recent series
A number of other mycobacteria have been
reported to cause disease in the HIV-infected patient.
Many of the clinical syndromes are similar to those
seen with MAC and can only be differentiated by
identification of the organism
Summary
The reduction in disseminated NTM infections
caused by HAART is one of the success stories in
the history of HIV in the developed world. Despite
this success, these diseases still occur and may have
atypical presentations in patients receiving HAART.
Clinicians treating HIV-infected patients must
remain familiar with the diagnosis and treatment of
these diseases and implement prevention strategies
when indicated.
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